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G. F. Combs

Publications and source records attributed to G. F. Combs.

4 recordsLinked to original sources
USGS1982

Biological effects of dietary T-2 toxin on rainbow trout, Salmo gairdneri

A 16-wk feeding study was conducted to evaluate the chronic toxicity of graded levels (0, 1.0, 2.5.5, 10 and 15 mg/kg of chemically pure dietary T-2 toxin (4,15-diacetoxy-8-(3-methylbutyryloxy)-12,13-epoxy-Δ 9 -tricothecen-3-ol) in 1-g rainbow trout, Salmo gairdneri , held in 9°C single-passage well water. Levels of T-2 toxin > 2.5 mg/kg depressed growth, efficiency of feed use, hematocrit, blood hemoglobin concentration and feed acceptance, and caused a transitory edema in a dose-dependent manner. Growth of trout fed a semipurified diet containing the toxin was described by the function: Y = 0.265 + 142.075 e (0.029 X 1 − 1.554x 2 3.7 ), where Y = gain as percentage starting weight per wk; X 1 is time in wk and 0 ⩽ X 1 ⩽16; and X 2 is T-2 content of diet in mg/kgand 0⩽ X 2 ⩽15. Exposure of fish to T-2 toxin did not affect activity of intestinal lumen chymoirypsin or trypsin, nitrogen digestibility or metabolizabte energy. Feeding of 15 mg/kg T-2 toxin to adult trout caused hemorrhaging in the intestines and regurgitation of subsequently intubated feed regardless of T-2 loxin content.

Aquatic Toxicology↗
USGS1976

Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): Gross, histological and biochemical deficiency signs

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 µg/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.

Journal of Nutrition↗